Celiac disease is a chronic immune-mediated disorder triggered by the ingestion of gluten in genetically susceptible individuals, primarily those carrying HLA-DQ2 or HLA-DQ8 and, in rare cases, HLA DQ7 alleles. Although traditionally regarded as a gastrointestinal condition, celiac disease is now recognized as a multisystem disorder with a wide range of clinical presentations. It has been described as a “clinical chameleon” due to its variable manifestations, which may include non-specific symptoms, extraintestinal involvement, or even an asymptomatic course, often identified only through screening of high-risk groups. This narrative review provides a comprehensive overview of celiac disease, highlighting recent insights into its pathogenesis, including genetic predisposition, immune mechanisms, and the role of environmental and microbial factors. It emphasizes the importance of recognizing extraintestinal features, outlines current diagnostic approaches and their limitations, and discusses management strategies centered around the gluten-free diet. Furthermore, it explores emerging therapies aimed at improving patient outcomes and reducing dependence on dietary restriction. By synthesizing the latest developments, this review aims to present a fresh perspective on a condition with significant clinical relevance that is evolving.

Exploring the role of genetic variants in susceptibility to autoimmune Diseases: A molecular genetics approach.

Disclosure: I.N. Rosa: None. L.A. Naves: None.Background. A variety of immune-related adverse events (irAE) have been described in patients under biologic treatment, specially immune checkpoints inhibitors (ICI). Although the impairment of pituitary function related to biological disease-modifying antirheumatic drugs (bDMARDs), as TNF-α inhibitors, is uncommon. We present a clinical case and discuss the potential mechanisms associated to immune and intracellular mediators as calcium regulation in pituitary during TNF-α inhibitor treatment. Clinical Case: A 27-year women presented at the Endocrinology Service, complaining of recurrent holocranial headache, fatigue, drowsiness and amenorrhea in the last six months. The patient had previous diagnosis of Psoriatic Arthritis and Hydroadenitis, under treatment with Adalimumab for 12 months. She presented a significant improvement of the inflammatory indexes (DAPSA, HAQ-DI, VAS, IHS4) on the first months of treatment, that remained stable during therapy. Hormonal evaluation suggested suppression of lactotrophic (PRL:4,3 ng/mL), somatotropic (IGF-1-1 SD) and gonadotropic axes FSH 0.5 mUI/mL; LH 0.07 mUI/mL; Oestradiol< 11 pg/mL, Testosterone 7ng/dL), since the third month of treatment; with integrity of corticotropic and thyrotrophic axes. MRI suggested a reduction on pituitary volume. Genetic predisposition was evaluated by investigation of HLA DQ2 e DQ8. Adalimumab was carried out and replaced by Secuquimumab. Hormonal evaluation was performed after 3 and 6 months, and a recovery of Lactotropic and Somatotropic axes was observed. Gonadotropic axes were still suppressed. Discussion and Conclusion: The hypothesis of TNF-α involvement in adenohypophysis hormone secretion was previously related to intracellular calcium mobilization, in experimental studies on prolactin and GH releases. Adalimumab is a recombinant monoclonal antibody involved in the inhibition of the binding of TNF-α to its receptors, p55 (TNFR1) and p75 (TNFR2), disrupting cytokine-driven inflammatory processes. In this case, central hypogonadism, and GH and prolactin secretion were transiently impaired during treatment with TNF-α inhibitors, reversible after Adalimumab replacement. The reduction in pituitary volume and gonadotropic, somatotropic and lactotropic axis may suggest hypophysitis, but TNF-α inhibitors can reduce intracellular Ca2+ and could interfere along the secretory pathway.Presentation: Sunday, July 13, 2025

Cerebrovascular diseases (CeVD) and neurodegenerative diseases (NDs) are two major neurological disorders, which are associated with increasing global morbidity and mortality. Population-based studies have indicated a complex link between CeVD and ND. However, the shared genetic etiology between these disease conditions remains less explored. We conducted genome-wide genetic correlation analysis and investigated the shared genetic architecture through pleiotropy analysis between ND and CeVD, like stroke and its subtypes, to understand shared genetic factors and biological mechanisms. Publicly available large-scale genome-wide association studies (GWAS) summary statistics data of cross-ancestry, European, and South Asian (SAS) ancestry were analyzed using methods implemented in the tools linkage disequilibrium score regression (LDSC), PLeiotropic Analysis under COmposite null hypothesis (PLACO), and Bayesian-based method of colocalization (COLOC). We detected 116 shared genetic loci consisting of 770 lead pleiotropic single nucleotide polymorphisms (SNPs) (ND-CeVD P-range: 4.81×10-8 to 4.57×10-16) and 40 shared causal genetic regions (ND-CeVD PP.H4-range: 0.70-0.9, posterior probability of H4 (PP.H4) ⩾ 0.7) between multiple CeVD and ND pairs. The genetic regions near ICA1L, HLA-DQA1, HLA-DRB1, MIR297, and PITX2 genes were identified as highly pleiotropic across multiple CeVD-ND pairs. We report ERGIC1 (5q35.1) for the first time as a shared causal genetic locus between Amyotrophic Lateral Sclerosis and small vessel stroke. The genetic risk score of stroke derived from the SAS population of the GIGASTROKE study was associated with ND (P-range = 2.23×10-28 to 0.02), despite a small sample size compared to other ethnic groups, indicating high penetrance. The shared genetic loci and pathway analysis in this study provide new genes and pathways shared between ND and CeVD, which may help in a better understanding of disease mechanisms in these neurological diseases.

Primary membranous nephropathy is a widely recognized autoimmune disease associated with podocyte antigens; the most important autoantigen is PLA2R1. PLA2R1 and HLA-DQA1 play important roles in the production of pathogenic antibodies. The purpose of this study was to observe the relationship between gene polymorphisms and primary membranous nephropathy and explore the clinical functional clues of PLA2R1 and HLA-DQA1 genes affecting treatment responsiveness. The study enrolled 89 patients with primary membranous nephropathy and 91 healthy people as a control. Single-nucleotide polymorphism loci (seven on PLA2R1 and two on HLA-DQA1) were identified using the PCR-Sanger technique. The patients were followed up until the 12th month, and relevant clinical data were collected. The relationship between these single-nucleotide polymorphism loci and primary membranous nephropathy remission was analyzed. Genotypic and allelic frequency distributions for six single-nucleotide polymorphisms within PLA2R1 (rs4664308, rs3792189, rs3792192, rs1870102, rs17831251, and rs35771982) and one in HLA-DQA1 (rs2187668) were associated with morbidity of primary membranous nephropathy. Single-nucleotide polymorphisms rs1870102, rs17831251, and rs2187668 were statistically significant in the genetic model analysis. The odds ratio for primary membranous nephropathy in patients carrying rs2187668 GG and rs1870102 AA was 52.875. We found that PLA2R1 single-nucleotide polymorphism rs36771982 was related to proteinuria remission at the 12th month, and found in further analysis that PLA2R1 single-nucleotide polymorphisms rs3792189, rs3792192, rs17831251, and rs35771982 were related to treatment response in the RTX group. In this study, we found several PLA2R1 and HLA-DQA1 single-nucleotide polymorphism loci associated with primary membranous nephropathy morbidity and that some PLA2R1 single-nucleotide polymorphism loci were related to the treatment response of patients with primary membranous nephropathy.

The D1Ce Screen pilot study stems from the Italian Republic Law 130/2023 introducing the screening based on autoantibody measurement on capillary blood for the identification of people in pre-symptomatic, early phase of type 1 diabetes (T1D) and/or having silent celiac disease (CD) in the general paediatric population to reduce the impact of the two more frequent and severe chronic diseases of childhood. Primary aim is to assess, on a smaller scale, the organizational feasibility, acceptability and sustainability by the National Health Service of the screening program to be conducted nationwide in Italy according to the law. This is an observational multicenter study, planning to screen 5,363 children from four Italian regions (Lombardy, Marche, Campania, Sardinia), proportionally distributed according to population of the single Regions, representative of the North, Centre, South and Islands of Italy. Participants are screened by autoantibodies within three classes of age 2-2.9, 6-6.9, and 10-10.9 years, corresponding to reported peaks of seroconversion, in order to maximize the identification of future cases of disease. HLA typing for HLA DQ2 and DQ8 is also performed for CD risk in dry blood spots (DBS). Screening procedures are conducted by primary care paediatricians (PCPs), responsible for: direct contact with families; information about the study; administration of written informed consent, privacy statement and questionnaires; execution of blood drawing by finger prick; capillary blood collection for autoantibody and HLA testing and shipment to the central laboratory. Feasibility, acceptability and sustainability will be estimated by number of participating paediatricians; screened children in the four Regions and within the classes of age; feedback questionnaires; number of fingerpicks to obtain sufficient capillary blood for assays; any adverse events; costs evaluation in relation to assigned budget. Secondary objectives include frequency of T1D and CD specific autoantibodies to assess the prevalence of pre-symptomatic (Stage 1 and Stage 2) TD1 and undiagnosed CD in the three classes of age of general paediatric population. D1Ce Screen is not registered to any International Study Registry, as it is a pilot observational study requested by the Italian law 130/2023.

BACKGROUND: In KhMAO-Yugra, every year there is an increase in the number of cases of type 1 diabetes mellitus (DM1) among residents of the district. The preservation of small indigenous peoples is an important demographic problem that requires an integrated approach. HLA-typing makes it possible to identify genetic markers of predisposition to type 1 diabetes mellitus (DM1) in the early stages of the disease and to ensure its prevention.AIM: Identification of the frequency of carriage of polymorphic alleles and haplotypes in the loci of the HLA-DQA1, HLA-DQB1 and HLA-DRB1 genes of the HLA class II system in samples of the indigenous khanty population and the alien population permanently residing in the territory of KhMAO-Yugra.MATERIALS AND METHODS. Low-resolution HLA typing was performed in 60 representatives of the khanty indigenous people, 54 conditionally healthy people of the alien population and 45 patients with type 1 diabetes mellitus (alien population) permanently residing in the territory of the Khanty-Mansiysk Autonomous Okrug.RESULTS: The analysis of the frequency of occurrence of class II HLA alleles in the khanty cohort revealed statistically significant differences in the alleles DQA1*01:02/03; DQB1*02; *03:02; *05:02/04; *06:01; *06:02-8; DRB1*03; *04; *12; *13; *15; *16 in comparison with the cohort of the conditionally healthy alien population. A similar comparison of the frequencies of DQA1, DQB1, DRB1 alleles, haplotypes and their combinations between representatives of the alien population of conditionally healthy and patients with DM1 revealed significant differences in loci DQA1*01:02/03; *03:01; DQB1*06:02-8; DRB1*07, characteristic of Caucasians. When comparing the frequencies of haplotypes in Hunts with a cohort of conditionally healthy newcomers, a statistically significant low frequency of haplotypes associated with a high and moderate risk of developing DM1 (DR4~DQ8, DR3~DQ2) and a high frequency of «protective» haplotypes DQ6~DR15, DQ6~DR13 were noted.CONCLUSION: In the khanty cohort, the frequency of occurrence of three haplotypes predisposing to the development of DM1 was reduced, and two protective haplotypes were increased, in comparison with the cohort of a conditionally healthy alien population. This determines the significant role of genetic factors in the observed low predisposition to the development of type 1 diabetes in the khanty population.

BackgroundGestational diabetes mellitus (GDM) is an endocrine disorder that occurs easily in women during pregnancy. HLA-DQA1/DQB1 genes play a crucial role in the regulation of the human immune and endocrine systems, potentially influencing the pathogenesis of GDM.ObjectiveTo explore the associations between single nucleotide polymorphisms (SNPs) in HLA-DQA1/DQB1 genes and the risk of GDM.MethodsSeven functional SNPs of HLA-DQA1/DQB1 genes were selected and genotyped in 523 GDM patients and 638 normal pregnant women. The odds ratio (OR) and its corresponding 95% confidence interval (CI) were utilized to assess the association between candidate SNPs and the risk of GDM. And then, false positive report probability (FPRP), multifactor dimensionality reduction (MDR) and haplotype analysis were employed to validate the statistically significant associations between studied SNPs and GDM risk.ResultsCompared to those with 0–1 risk genotypes, individuals with 2–7 unfavorable genotypes presented an increased risk of GDM (adjusted OR = 1.54, 95% CI=1.04-2.28, P=0.033). A dose- accumulation effect was detected between the number of unfavorable genotypes and GDM risk (Ptrend=0.024). Furthermore, stratified analysis revealed that the increased GDM risk was more likely to occur in individuals with higher blood pressure and TG, and lower HDL-c levels (P<0.05). Multifactor dimensionality reduction (MDR) analysis revealed that rs9274666 was the best single locus model, whereas the 7-loci model was the best multifactor interaction model for predicting GDM risk (χ²=134.28, P<0.0001). Finally, haplotype analysis revealed that the ACGAGTA and ACGGATA haplotypes were significantly associated with the increased GDM risk. HLA-DQA1/DQB1 SNPs can significantly alter individuals’ genetic susceptibility to GDM.ConclusionsThe genetic variations in the HLA-DQA1 and HLA-DQB1 genes may collectively contribute to the susceptibility to gestational diabetes mellitus. These findings suggest that these genetic markers could be useful for early prediction of GDM, and further validation in larger cohorts is warranted.

Multiple sclerosis (MS), which can lead to severe physical or cognitive disability and neurological deficits, is a chronic autoimmune disease affecting the central nervous system (CNS). The etiology and pathogenesis of MS remain unclear; nonetheless, it is asserted that its cause is complex, with genetic predisposition playing a significant role. In this study, our aim was to analyze the relationship between MS and HLA-DRA (rs3135388 and rs3135391), HLA-DQA1 (rs9272346) and IL-6 (rs1800795 and rs1900796) gene polymorphisms, which play an important role in inflammation and immune response. The study included 100 healthy controls and 98 MS patients. Real-time polymerase chain reaction (RT-PCR) was used to analyze variations in rs3135388 and rs3135391 in the HLA-DRA gene, rs9272346 in the HLA-DQA1 gene, and rs1800795 and rs1900796 in the IL-6 gene following DNA isolation from peripheral blood. Statistical techniques were applied to assess the outcomes. The results showed a significant difference in IL-6 (rs1800796) G/C (p = 0.024) between the patient and control groups when genotypes and allele distributions were analyzed. HLA-DQA1 (rs9272346) and HLA-DRA (rs3135388 and rs3135391) variations did not substantially differ between the two groups. Similarly, no significant difference was found between the two groups in VitD, B12 and folic acid parameters, and there was no relationship between these parameters and genotypes. There is evidence suggesting a significant association between IL-6 (rs1800796) polymorphisms and MS. IL-6 (rs1800796) GC genotype may be associated with disease susceptibility or risk. This should be taken into account in association and intervention studies on MS.

BackgroundProactive therapeutic drug monitoring facilitates early dose optimization to prevent primary and secondary failure to antitumor necrosis factor (TNF). We aimed to investigate the impact of dashboard-guided induction dosing strategy on anti-TNF durability and immunogenicity.MethodsWe conducted a single-center cohort analysis of patients with Crohn’s disease (CD) and Ulcerative colitis (UC) who initiated treatment with infliximab or adalimumab between January 2020 and March 2023. Induction was prospectively personalized using a pharmacokinetic model-guided dosing strategy, with drug measurements at week 2, 6, and 14, and the first dose adjustment occurred in week 4. Data were recorded retrospectively. We assessed treatment durability, pharmacokinetic outcomes, clinical remission (CR), and endoscopic remission (ER), at both weeks 24 and 56. Multivariate analysis and Kaplan–Meier curves were used to compare outcomes.ResultsWe enrolled 147 patients (92 CD /55 UC). Anti-TNF drug survival probability was 85.00% after a year. Seventy-seven percent of patients were prescribed an intensified dose in the first year, which was associated with improved drug durability. Only 1 patient out of 147 developed antibodies to adalimumab, none to infliximab. After 24 and 52 weeks of treatment 92.5% (136/147) and 72.78% (107/147) of patients achieved CR, respectively. ER was observed in 59.39% (79/133) of patients. The use of immunomodulators or carriage of HLA DQA1*05 variant was not associated with adverse treatment or pharmacokinetic outcomes.ConclusionsOptimizing anti-TNF induction with a dashboard-guide dosing strategy proves to be a valuable approach to enhance treatment durability and clinical outcomes in inflammatory bowel disease patients. Immunogenicity appears to be mitigated by the model, which even mitigates the impact of immunomodulators and overcomes HLA DQA1*05 effect.

Background. Celiac Disease (CD) is an autoimmune disorder triggered by gluten ingestion, leading to small intestine damage and potential malnutrition. CD has a strong genetic basis, primarily linked to specific Human Leukocyte Antigen (HLA) gene variants, especially HLA-DQ2 and HLA-DQ8, essential in presenting gluten peptides to immune cells. Objective. The study aims to evaluate the molecular detection of HLA-DQA1, HLA-DQB1, and Tissue Transglutaminase (TGM2) genes by using conventional PCR technique with specific primers in CD patients. Additionally, DNA sequencing of these genes was performed to compare them with standard genes to detect Single Nucleotide Polymorphisms (SNPs) occurring in the studied genes. Methodology. This study used a case-control design with 118 total participants, of whom 68 were newly diagnosed CD patients, while 50 comprised the control group. Participants were recruited from various teaching hospitals in Al-Basrah, Iraq, from December 2023 to June 2024. Fifteen samples were analyzed, with five for each primer used for DNA sequencing. PCR and Sanger sequencing were performed to detect genetic polymorphisms, and the novel DNA sequences were aligned with the NCBI reference sequences to verify the presence of SNPs. Results. The study identified ten SNPs in the HLA-DQA1 gene, one SNP in the HLA-DQB1 gene, and four SNPs in the TGM2 gene. These SNPs exhibited different zygosity states, with HLA-DQA1 showing both homozygous and heterozygous forms. Conclusion. The dbSNP database confirmed these detected polymorphisms, enhancing the understanding of genetic variation in CD-associated genes. This research supports the necessity of genetic testing for identifying CD predisposition and contributes to further genomic and clinical investigations of autoimmune diseases.

Multiple sclerosis (MS) is among the most common autoimmune disorders and is characterized by inflammation and degeneration affecting the central nervous system. Glatiramer acetate (GA) is an immunomodulatory drug utilized for treating relapsing-remitting MS. However, a considerable number of patients do not exhibit an appropriate response to this drug. This condition is known as GA resistance. This study aimed to investigate the relationship between nucleotide variations in the HLA-DRA, HLA-DQA1 and IL-6 genes and GA resistance. Additionally, the relationship of environmental factors with MS was investigated. One hundred thirty-nine MS patients were enrolled in this study. Patients were divided into two groups: non-responders (n = 58) and responders (n = 81). After DNA was isolated from peripheral blood, the rs3135388 and rs3135391 variations in HLA-DRA, the rs9272346 variation in HLA-DQA1, and the rs1800795 and rs1900796 variations in IL-6 were analyzed by Real-Time Polymerase Chain Reaction (RT-PCR). At the end of the study, it was found that the number of females was approximately 3 times greater in responders and 4 times greater in non-responders than in males. When nucleotide variations and allele distributions were compared between the groups, no significant relationships were found. Similarly, no significant relationship was found between risk factors and nucleotide variations. However, in non-responders, the expanded disability status scale and lesion load were found to be significantly high. In conclusion, by increasing the number of patients, more meaningful results can be achieved in future studies. Elucidating the pharmacogenetic characteristics (the drug-gene relationship) of MS patients using GA could lead to the development of personalized treatment strategies.

Celiac disease is defined as a systemic immunological disorder caused by gluten (gliadin and other prolamin) in genetically predisposed individuals, who present with a variety of gluten-dependent symptoms, specific antibodies, the presence of the HLA DQ2 and DQ8 histocompatibility antigen, and enteropathy. Its prevalence, depending on the studied population and methodology, is estimated at 0.75-1.6% of the general population. During the complex immune reaction it induces, most cells involved in inflammatory processes are activated, which leads to the gradual atrophy of intestinal villi and the proliferation of enterocytes within intestinal crypts. The pathogenesis of celiac disease is extremely complicated and is still the subject of research. According to the current diagnostic guidelines, the following criteria should be taken into account: clinical symptoms (intestinal and extraintestinal), the presence of antibodies against tissue transglutaminase in the IgA class, the level of total IgA, and the presence of typical histological changes in duodenal biopsies. Diet-resistant celiac disease is one of the most important clinical challenges, causing serious complications. Currently, the basic method for treating celiac disease is an elimination diet (i.e., the exclusion of products that may contain gluten from the diet), however, new therapeutic strategies are still being sought, mainly based on supplementation with exogenous endopeptidases, modification of the immune response, and the use of zonulin inhibitors and transglutaminase 2 inhibitors. Clinical trials of new drugs are ongoing. The gradually expanding knowledge about the pathogenesis of celiac disease may allow for the development of new therapeutic strategies for both patients with a mild disease course, as well as those that are diet-resistant.

HLA-DR genes are associated with the progression from stage 1 and stage 2 to onset of stage 3 type 1 diabetes (T1D), after accounting HLA-DQ genes with which they are in high linkage disequilibrium. Based on an integrated cohort of participants from 2 completed clinical trials, this investigation finds that, sharing a haplotype with the DRB1*03:01 (DR3) allele, DRB3*01:01:02 and *02:02:01 have respectively negative and positive associations with the progression. Furthermore, we uncovered 2 residues (β11, β26, participating in pockets 6 and 4, respectively) on the DRB3 molecule responsible for the progression among DR3 carriers; motif RY and LF respectively delay and promote the progression (hazard ratio [HR] = 0.73 and 2.38, P = 0.039 and 0.017, respectively). Two anchoring pockets 6 and 4 probably bind differential autoantigenic epitopes. We further investigated the progression association with the motifs RY and LF among carriers of DR3 and found that carriers of the motif LF have significantly faster progression than carriers of RY (HR = 1.48, P = 0.019 in unadjusted analysis; HR = 1.39, P = 0.047 in adjusted analysis), results of which provide an impetus to examine the possible role of specific DRB3-binding peptides in the progression to T1D.

Although numerous candidate genes have been identified in studies investigating the role of genetics in sarcoidosis, the strongest association has been reported with the Major Histocompatibility Complex/Human Leucocyte Antigen (MHC/HLA) region. This study aimed to evaluate HLA polymorphism and assess its association with cardiac and other extrapulmonary involvement in sarcoidosis patients. The study included 67 patients diagnosed with sarcoidosis. A control group of 100 bone marrow donors, who had undergone HLA genotyping previously, was also included. Blood samples were collected from all participants for HLA gene polymorphism analysis. The differences in HLA genotypes were investigated between patients with and without cardiac and other extrapulmonary involvement, and between these groups and the control group. Cardiac involvement, was present in 17.9% of the patients. The most frequently affected extrapulmonary organ was the skin (23.8%). HLA DQB103 and HLA DQB106 alleles were expressed more frequently in patients with only pulmonary involvement compared to those with extrapulmonary involvement. Conversely, HLA DQA101 was expressed more frequently in patients with extrapulmonary involvement. No statistically significant difference in the expression of HLA DRB1, HLA DQB1, and HLA DQA1 alleles was observed between sarcoidosis patients with and without cardiac involvement. Our findings suggest that HLA DQB103 and HLA DQB106 alleles might be protective against extrapulmonary organ involvement, while HLA DQA101 could be a risk factor. These findings may contribute to the prediction of treatment response and prognosis in sarcoidosis patients.

Introduction: In Asia, chronic hepatitis B is one of the most prevalent infectious diseases affecting public health. Studying the genetic polymorphism of human leukocyte antigen (HLA) is one of the influencing factors in the progression and development of this disease. Most studies have examined the association between HLA-DQ and hepatitis B virus (HBV) infection/clearance, disease progression, and chronic hepatitis B virus infection (CHB) complications. Objectives: This study investigated the effect of rs2856718 and rs9275572 polymorphisms on HBV patients and healthy individuals. Materials and Methods: In this study, rs2856718 and rs9275572 were analyzed in 60 patients with chronic hepatitis B and 60 healthy individuals using the tetra-primer amplification refractory mutation system-polymerase chain reaction (TETRA-ARMS-PCR) method. Results: In this case-control study, 60 patients with CHB, consisting of 43 males and 17 females (71.7% male; 28.3% female; mean: 39.25 ± 9.67 years), and 60 healthy individuals, consisting of 16 males and 44 females (26.7% male; 73.3% female; mean: 32.98 ± 9.58 years), were enrolled. The results indicated that HLA-DQ recessive models, including rs2856718 (OR: 3.281; P = 0.007) and rs9275572 (OR: 5.8; P = 0.015), significantly increased risk, whereas the rs2856718 co-dominant model (OR: 0.357, P = 0.006) correlated with a decreased risk of CHB virus infection. Conclusion: The results can aid in identifying individuals at risk of HBV infection. The findings may indicate that the HLA-II gene in the host is a determining factor in the outcome of hepatitis B infection. Thus, studying these polymorphisms is recommended, especially in advanced liver disease.

OP06 HLA-DQA1*05:01 is associated with loss of response to infliximab, and HLA DQA1*05:05 with loss of response to adalimumab in the Oxford OASIS study

P0495 Impact of the HLA DQA1*05 allele on the efficacy of vedolizumab treatment in inflammatory bowel disease

N11 Switching from intravenous to subcutaneous infliximab enhances trough levels and can facilitate de-escalation of concomitant immunomodulation, irrespective of the HLA DQA1*05 status: a prospective real-world study

P0002 Identification of Infliximab and Adalimumab -derived peptides using MHC class II antibody mediated immunopeptidomics and mass spectrometry: implications for drug re-design